Heme oxygenase-1 alleviated non-alcoholic fatty liver disease via suppressing ROS-dependent endoplasmic reticulum stress
The endoplasmic reticulum (ER) stress response plays a crucial role in the development of nonalcoholic steatohepatitis (NASH). Heme oxygenase-1 (HO-1) exerts beneficial effects against oxidative injury in NASH. This study is aimed to clarify whether HO-1 is an effective therapeutic strategy for NASH...
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| Veröffentlicht in: | Life sciences (1973) 2020-07, Vol.253, p.117678-11, Article 117678 |
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| creator | Li, Dongdong Zhao, Dandan Du, Jinghua Dong, Shiming Aldhamin, Zaid Yuan, Xiwei Li, Wencong Du, Huijuan Zhao, Wen Cui, Luyao Liu, Lingdi Fu, Na Nan, Yuemin |
| description | The endoplasmic reticulum (ER) stress response plays a crucial role in the development of nonalcoholic steatohepatitis (NASH). Heme oxygenase-1 (HO-1) exerts beneficial effects against oxidative injury in NASH. This study is aimed to clarify whether HO-1 is an effective therapeutic strategy for NASH via regulation of ER stress.
The C57BL/6J mice were fed with methionine-choline deficient (MCD) for 4 weeks and high fat-high carbohydrate-high cholesterol (HFD) diet for 16 weeks, with hemin or zinc protoporphyrin IX (ZnPP-IX), respectively. The LO-2 cells were cultured in palmitic medium, with transfected pEX-HO-1 or sh-HO-1 plasmid for 24 h. Meanwhile, thirty NASH patients and 15 health controls were enrolled. The ER ultrastructure was observed by transmission electron microscopy (TEM) and confocal microscopy. The expressions of mRNAs and proteins of HO-1, ER stress related genes were detected by real time PCR, western blot and immunohistochemical staining, respectively.
The swelled and broken rough endoplasmic reticulums were observed in MCD and HFD fed mice. The reactive hepatic expression of HO-1 was related with the increased ROS production and ER stress, companied with upregulation of GRP78, p-IRE1, PERK, ATF6. Through hemin administration, hepatocyte apoptosis was suppressed companied down-regulation of CHOP, caspase12 and up-regulation of BCL2. Conserved results were exhibited in ZnPP-IX administrated mice and HO-1 silent cells. Consistent results were observed in the NASH Patients.
HO-1 could serve as a protective factor in the progression of nutritional steatohepatitis by suppresses hepatocyte excessive ER stress and might be a potential target for therapy of nonalcoholic steatohepatitis.
•The endoplasmic reticulum stress response plays a crucial role in the development of nonalcoholic steatohepatitis.•The swelled and broken rough endoplasmic reticulums were observed in diet-induced steatohepatitis•Heme oxygenase-1 serve as a protective factor in the progression of nutritional steatohepatitis.•Heme oxygenase-1 suppresses hepatocyte excessive ER stress in nonalcoholic steatohepatitis |
| doi_str_mv | 10.1016/j.lfs.2020.117678 |
| format | Article |
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The C57BL/6J mice were fed with methionine-choline deficient (MCD) for 4 weeks and high fat-high carbohydrate-high cholesterol (HFD) diet for 16 weeks, with hemin or zinc protoporphyrin IX (ZnPP-IX), respectively. The LO-2 cells were cultured in palmitic medium, with transfected pEX-HO-1 or sh-HO-1 plasmid for 24 h. Meanwhile, thirty NASH patients and 15 health controls were enrolled. The ER ultrastructure was observed by transmission electron microscopy (TEM) and confocal microscopy. The expressions of mRNAs and proteins of HO-1, ER stress related genes were detected by real time PCR, western blot and immunohistochemical staining, respectively.
The swelled and broken rough endoplasmic reticulums were observed in MCD and HFD fed mice. The reactive hepatic expression of HO-1 was related with the increased ROS production and ER stress, companied with upregulation of GRP78, p-IRE1, PERK, ATF6. Through hemin administration, hepatocyte apoptosis was suppressed companied down-regulation of CHOP, caspase12 and up-regulation of BCL2. Conserved results were exhibited in ZnPP-IX administrated mice and HO-1 silent cells. Consistent results were observed in the NASH Patients.
HO-1 could serve as a protective factor in the progression of nutritional steatohepatitis by suppresses hepatocyte excessive ER stress and might be a potential target for therapy of nonalcoholic steatohepatitis.
•The endoplasmic reticulum stress response plays a crucial role in the development of nonalcoholic steatohepatitis.•The swelled and broken rough endoplasmic reticulums were observed in diet-induced steatohepatitis•Heme oxygenase-1 serve as a protective factor in the progression of nutritional steatohepatitis.•Heme oxygenase-1 suppresses hepatocyte excessive ER stress in nonalcoholic steatohepatitis</description><identifier>ISSN: 0024-3205</identifier><identifier>EISSN: 1879-0631</identifier><identifier>DOI: 10.1016/j.lfs.2020.117678</identifier><identifier>PMID: 32376267</identifier><language>eng</language><publisher>Netherlands: Elsevier Inc</publisher><subject>Apoptosis ; Carbohydrates ; Cholesterol ; Choline ; Confocal microscopy ; Endoplasmic reticulum ; Endoplasmic reticulum stress ; Fatty liver ; Heme ; Heme oxygenase (decyclizing) ; Heme oxygenase-1 ; Hemin ; High carbohydrate diet ; High cholesterol diet ; Liver diseases ; Methionine ; Microscopy ; Non-alcoholic fatty liver disease ; Oxygenase ; Protoporphyrin ; Protoporphyrin IX ; Reactive oxygen species ; Transmission electron microscopy ; Ultrastructure ; Zinc protoporphyrin IX</subject><ispartof>Life sciences (1973), 2020-07, Vol.253, p.117678-11, Article 117678</ispartof><rights>2020 Elsevier Inc.</rights><rights>Copyright © 2020 Elsevier Inc. All rights reserved.</rights><rights>Copyright Elsevier BV Jul 15, 2020</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c381t-68a6603b865b7e20203cbeadca00c707535297f6f8f85147e7f669a658175c573</citedby><cites>FETCH-LOGICAL-c381t-68a6603b865b7e20203cbeadca00c707535297f6f8f85147e7f669a658175c573</cites><orcidid>0000-0002-0503-2592 ; 0000-0001-6061-4205</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S0024320520304264$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,776,780,3537,27901,27902,65306</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/32376267$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Li, Dongdong</creatorcontrib><creatorcontrib>Zhao, Dandan</creatorcontrib><creatorcontrib>Du, Jinghua</creatorcontrib><creatorcontrib>Dong, Shiming</creatorcontrib><creatorcontrib>Aldhamin, Zaid</creatorcontrib><creatorcontrib>Yuan, Xiwei</creatorcontrib><creatorcontrib>Li, Wencong</creatorcontrib><creatorcontrib>Du, Huijuan</creatorcontrib><creatorcontrib>Zhao, Wen</creatorcontrib><creatorcontrib>Cui, Luyao</creatorcontrib><creatorcontrib>Liu, Lingdi</creatorcontrib><creatorcontrib>Fu, Na</creatorcontrib><creatorcontrib>Nan, Yuemin</creatorcontrib><title>Heme oxygenase-1 alleviated non-alcoholic fatty liver disease via suppressing ROS-dependent endoplasmic reticulum stress</title><title>Life sciences (1973)</title><addtitle>Life Sci</addtitle><description>The endoplasmic reticulum (ER) stress response plays a crucial role in the development of nonalcoholic steatohepatitis (NASH). Heme oxygenase-1 (HO-1) exerts beneficial effects against oxidative injury in NASH. This study is aimed to clarify whether HO-1 is an effective therapeutic strategy for NASH via regulation of ER stress.
The C57BL/6J mice were fed with methionine-choline deficient (MCD) for 4 weeks and high fat-high carbohydrate-high cholesterol (HFD) diet for 16 weeks, with hemin or zinc protoporphyrin IX (ZnPP-IX), respectively. The LO-2 cells were cultured in palmitic medium, with transfected pEX-HO-1 or sh-HO-1 plasmid for 24 h. Meanwhile, thirty NASH patients and 15 health controls were enrolled. The ER ultrastructure was observed by transmission electron microscopy (TEM) and confocal microscopy. The expressions of mRNAs and proteins of HO-1, ER stress related genes were detected by real time PCR, western blot and immunohistochemical staining, respectively.
The swelled and broken rough endoplasmic reticulums were observed in MCD and HFD fed mice. The reactive hepatic expression of HO-1 was related with the increased ROS production and ER stress, companied with upregulation of GRP78, p-IRE1, PERK, ATF6. Through hemin administration, hepatocyte apoptosis was suppressed companied down-regulation of CHOP, caspase12 and up-regulation of BCL2. Conserved results were exhibited in ZnPP-IX administrated mice and HO-1 silent cells. Consistent results were observed in the NASH Patients.
HO-1 could serve as a protective factor in the progression of nutritional steatohepatitis by suppresses hepatocyte excessive ER stress and might be a potential target for therapy of nonalcoholic steatohepatitis.
•The endoplasmic reticulum stress response plays a crucial role in the development of nonalcoholic steatohepatitis.•The swelled and broken rough endoplasmic reticulums were observed in diet-induced steatohepatitis•Heme oxygenase-1 serve as a protective factor in the progression of nutritional steatohepatitis.•Heme oxygenase-1 suppresses hepatocyte excessive ER stress in nonalcoholic steatohepatitis</description><subject>Apoptosis</subject><subject>Carbohydrates</subject><subject>Cholesterol</subject><subject>Choline</subject><subject>Confocal microscopy</subject><subject>Endoplasmic reticulum</subject><subject>Endoplasmic reticulum stress</subject><subject>Fatty liver</subject><subject>Heme</subject><subject>Heme oxygenase (decyclizing)</subject><subject>Heme oxygenase-1</subject><subject>Hemin</subject><subject>High carbohydrate diet</subject><subject>High cholesterol diet</subject><subject>Liver diseases</subject><subject>Methionine</subject><subject>Microscopy</subject><subject>Non-alcoholic fatty liver disease</subject><subject>Oxygenase</subject><subject>Protoporphyrin</subject><subject>Protoporphyrin IX</subject><subject>Reactive oxygen species</subject><subject>Transmission electron microscopy</subject><subject>Ultrastructure</subject><subject>Zinc protoporphyrin IX</subject><issn>0024-3205</issn><issn>1879-0631</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2020</creationdate><recordtype>article</recordtype><recordid>eNp9kU2LFDEQhoMo7jj6A7xIwIuXHvMx-Wg8ybK6wsKCH-eQSVevGdJJm6SHnX9vhtn1sAdPVQXP-1JVL0JvKdlQQuXH_SaMZcMIazNVUulnaEW16jsiOX2OVoSwbccZERfoVSl7QogQir9EF5xxJZlUK3R_DRPgdH-8g2gLdBTbEODgbYUBxxQ7G1z6nYJ3eLS1HnHwB8h48AUajhuIyzLPGUrx8Q5_v_3RDTBDHCBW3Eqagy1TU2eo3i1hmXCpJ_o1ejHaUODNQ12jX1-ufl5edze3X79dfr7pHNe0dlJbKQnfaSl2Ck6ncrcDOzhLiFNECS5Yr0Y56lELulXQetlbKTRVwrVr1-jD2XfO6c8CpZrJFwch2AhpKYbxvtec0vayNXr_BN2nJce2nWFbJbXYUi4aRc-Uy6mUDKOZs59sPhpKzCkWszctFnPa1ZxjaZp3D87LboLhn-IxhwZ8OgPQXnHwkE1xHqKDwWdw1QzJ_8f-L8Lanc0</recordid><startdate>20200715</startdate><enddate>20200715</enddate><creator>Li, Dongdong</creator><creator>Zhao, Dandan</creator><creator>Du, Jinghua</creator><creator>Dong, Shiming</creator><creator>Aldhamin, Zaid</creator><creator>Yuan, Xiwei</creator><creator>Li, Wencong</creator><creator>Du, Huijuan</creator><creator>Zhao, Wen</creator><creator>Cui, Luyao</creator><creator>Liu, Lingdi</creator><creator>Fu, Na</creator><creator>Nan, Yuemin</creator><general>Elsevier Inc</general><general>Elsevier BV</general><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7QP</scope><scope>7QR</scope><scope>7TK</scope><scope>7U7</scope><scope>7U9</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>H94</scope><scope>P64</scope><scope>RC3</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0002-0503-2592</orcidid><orcidid>https://orcid.org/0000-0001-6061-4205</orcidid></search><sort><creationdate>20200715</creationdate><title>Heme oxygenase-1 alleviated non-alcoholic fatty liver disease via suppressing ROS-dependent endoplasmic reticulum stress</title><author>Li, Dongdong ; Zhao, Dandan ; Du, Jinghua ; Dong, Shiming ; Aldhamin, Zaid ; Yuan, Xiwei ; Li, Wencong ; Du, Huijuan ; Zhao, Wen ; Cui, Luyao ; Liu, Lingdi ; Fu, Na ; Nan, Yuemin</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c381t-68a6603b865b7e20203cbeadca00c707535297f6f8f85147e7f669a658175c573</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2020</creationdate><topic>Apoptosis</topic><topic>Carbohydrates</topic><topic>Cholesterol</topic><topic>Choline</topic><topic>Confocal microscopy</topic><topic>Endoplasmic reticulum</topic><topic>Endoplasmic reticulum stress</topic><topic>Fatty liver</topic><topic>Heme</topic><topic>Heme oxygenase (decyclizing)</topic><topic>Heme oxygenase-1</topic><topic>Hemin</topic><topic>High carbohydrate diet</topic><topic>High cholesterol diet</topic><topic>Liver diseases</topic><topic>Methionine</topic><topic>Microscopy</topic><topic>Non-alcoholic fatty liver disease</topic><topic>Oxygenase</topic><topic>Protoporphyrin</topic><topic>Protoporphyrin IX</topic><topic>Reactive oxygen species</topic><topic>Transmission electron microscopy</topic><topic>Ultrastructure</topic><topic>Zinc protoporphyrin IX</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Li, Dongdong</creatorcontrib><creatorcontrib>Zhao, Dandan</creatorcontrib><creatorcontrib>Du, Jinghua</creatorcontrib><creatorcontrib>Dong, Shiming</creatorcontrib><creatorcontrib>Aldhamin, Zaid</creatorcontrib><creatorcontrib>Yuan, Xiwei</creatorcontrib><creatorcontrib>Li, Wencong</creatorcontrib><creatorcontrib>Du, Huijuan</creatorcontrib><creatorcontrib>Zhao, Wen</creatorcontrib><creatorcontrib>Cui, Luyao</creatorcontrib><creatorcontrib>Liu, Lingdi</creatorcontrib><creatorcontrib>Fu, Na</creatorcontrib><creatorcontrib>Nan, Yuemin</creatorcontrib><collection>PubMed</collection><collection>CrossRef</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Chemoreception Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Toxicology Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Technology Research Database</collection><collection>Environmental Sciences and Pollution Management</collection><collection>Engineering Research Database</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Life sciences (1973)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Li, Dongdong</au><au>Zhao, Dandan</au><au>Du, Jinghua</au><au>Dong, Shiming</au><au>Aldhamin, Zaid</au><au>Yuan, Xiwei</au><au>Li, Wencong</au><au>Du, Huijuan</au><au>Zhao, Wen</au><au>Cui, Luyao</au><au>Liu, Lingdi</au><au>Fu, Na</au><au>Nan, Yuemin</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Heme oxygenase-1 alleviated non-alcoholic fatty liver disease via suppressing ROS-dependent endoplasmic reticulum stress</atitle><jtitle>Life sciences (1973)</jtitle><addtitle>Life Sci</addtitle><date>2020-07-15</date><risdate>2020</risdate><volume>253</volume><spage>117678</spage><epage>11</epage><pages>117678-11</pages><artnum>117678</artnum><issn>0024-3205</issn><eissn>1879-0631</eissn><abstract>The endoplasmic reticulum (ER) stress response plays a crucial role in the development of nonalcoholic steatohepatitis (NASH). Heme oxygenase-1 (HO-1) exerts beneficial effects against oxidative injury in NASH. This study is aimed to clarify whether HO-1 is an effective therapeutic strategy for NASH via regulation of ER stress.
The C57BL/6J mice were fed with methionine-choline deficient (MCD) for 4 weeks and high fat-high carbohydrate-high cholesterol (HFD) diet for 16 weeks, with hemin or zinc protoporphyrin IX (ZnPP-IX), respectively. The LO-2 cells were cultured in palmitic medium, with transfected pEX-HO-1 or sh-HO-1 plasmid for 24 h. Meanwhile, thirty NASH patients and 15 health controls were enrolled. The ER ultrastructure was observed by transmission electron microscopy (TEM) and confocal microscopy. The expressions of mRNAs and proteins of HO-1, ER stress related genes were detected by real time PCR, western blot and immunohistochemical staining, respectively.
The swelled and broken rough endoplasmic reticulums were observed in MCD and HFD fed mice. The reactive hepatic expression of HO-1 was related with the increased ROS production and ER stress, companied with upregulation of GRP78, p-IRE1, PERK, ATF6. Through hemin administration, hepatocyte apoptosis was suppressed companied down-regulation of CHOP, caspase12 and up-regulation of BCL2. Conserved results were exhibited in ZnPP-IX administrated mice and HO-1 silent cells. Consistent results were observed in the NASH Patients.
HO-1 could serve as a protective factor in the progression of nutritional steatohepatitis by suppresses hepatocyte excessive ER stress and might be a potential target for therapy of nonalcoholic steatohepatitis.
•The endoplasmic reticulum stress response plays a crucial role in the development of nonalcoholic steatohepatitis.•The swelled and broken rough endoplasmic reticulums were observed in diet-induced steatohepatitis•Heme oxygenase-1 serve as a protective factor in the progression of nutritional steatohepatitis.•Heme oxygenase-1 suppresses hepatocyte excessive ER stress in nonalcoholic steatohepatitis</abstract><cop>Netherlands</cop><pub>Elsevier Inc</pub><pmid>32376267</pmid><doi>10.1016/j.lfs.2020.117678</doi><tpages>11</tpages><orcidid>https://orcid.org/0000-0002-0503-2592</orcidid><orcidid>https://orcid.org/0000-0001-6061-4205</orcidid></addata></record> |
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| subjects | Apoptosis Carbohydrates Cholesterol Choline Confocal microscopy Endoplasmic reticulum Endoplasmic reticulum stress Fatty liver Heme Heme oxygenase (decyclizing) Heme oxygenase-1 Hemin High carbohydrate diet High cholesterol diet Liver diseases Methionine Microscopy Non-alcoholic fatty liver disease Oxygenase Protoporphyrin Protoporphyrin IX Reactive oxygen species Transmission electron microscopy Ultrastructure Zinc protoporphyrin IX |
| title | Heme oxygenase-1 alleviated non-alcoholic fatty liver disease via suppressing ROS-dependent endoplasmic reticulum stress |
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